Neuroprotection refers to the relative preservation of neuronal structure and/or function.[1] In the case of an ongoing insult (a neurodegenerative insult) the relative preservation of neuronal integrity implies a reduction in the rate of neuronal loss over time, which can be expressed as a differential equation.[1][2]
Despite differences in symptoms or injuries associated with CNS disorders, many of the mechanisms behind neurodegeneration are the same. Common mechanisms of neuronal injury include decreased delivery of oxygen and glucose to the brain, energy failure, increased levels in oxidative stress, mitochondrial dysfunction, excitotoxicity, inflammatory changes, iron accumulation, and protein aggregation.[4][3][5][6] Of these mechanisms, neuroprotective treatments often target oxidative stress and excitotoxicity—both of which are highly associated with CNS disorders. Not only can oxidative stress and excitotoxicity trigger neuron cell death but when combined they have synergistic effects that cause even more degradation than on their own.[7] Thus limiting excitotoxicity and oxidative stress is a very important aspect of neuroprotection. Common neuroprotective treatments are glutamate antagonists and antioxidants, which aim to limit excitotoxicity and oxidative stress respectively.
^Dunnett SB, Björklund A (June 1999). "Prospects for new restorative and neuroprotective treatments in Parkinson's disease". Nature. 399 (6738 Suppl): A32–A39. doi:10.1038/399a032. PMID10392578. S2CID17462928.
^Andersen JK (July 2004). "Oxidative stress in neurodegeneration: cause or consequence?". Nature Medicine. 10 Suppl (7): S18–S25. doi:10.1038/nrn1434. PMID15298006. S2CID9569296.
^Zádori D, Klivényi P, Szalárdy L, Fülöp F, Toldi J, Vécsei L (November 2012). "Mitochondrial disturbances, excitotoxicity, neuroinflammation and kynurenines: novel therapeutic strategies for neurodegenerative disorders". Journal of the Neurological Sciences. 322 (1–2): 187–191. doi:10.1016/j.jns.2012.06.004. PMID22749004. S2CID25867213.